Esinduy C B, Chang C C, Trosko J E, Ruch R J
Department of Pathology, Medical College of Ohio, Toledo 43699.
Carcinogenesis. 1995 Apr;16(4):915-21. doi: 10.1093/carcin/16.4.915.
We examined whether the inhibition of neoplastically transformed cell growth by co-cultured non-transformed cells involved gap junctional intercellular communication (GJIC). The growth of poorly communicating (approximately 25-35% dye-coupled cells), Ha-ras and neu oncogene-transformed WB-F344 rat liver epithelial cells was inhibited by co-culture with highly communicating (90-95% dye-coupling), non-transformed WB-F344 cells. Inhibition was dependent upon heterologous cell-cell contact and required that the non-transformed cells were GJIC competent. GJIC-deficient mutant WB-F344 cells did not suppress transformed cell growth. Restoration of mutant cell GJIC by transfection with rat connexin43 cDNA restored growth-inhibiting activity. These results clearly demonstrate a role for GJIC in the inhibition of transformed cell growth by non-transformed cells.
我们研究了共培养的未转化细胞对肿瘤转化细胞生长的抑制作用是否涉及间隙连接细胞间通讯（GJIC）。将低通讯性（约25 - 35%染料偶联细胞）、Ha-ras和neu癌基因转化的WB-F344大鼠肝上皮细胞与高通讯性（90 - 95%染料偶联）的未转化WB-F344细胞共培养，可抑制其生长。抑制作用依赖于异源细胞间接触，且要求未转化细胞具有GJIC能力。GJIC缺陷的突变型WB-F344细胞不能抑制转化细胞的生长。通过用大鼠连接蛋白43 cDNA转染恢复突变细胞的GJIC，可恢复其生长抑制活性。这些结果清楚地证明了GJIC在未转化细胞对转化细胞生长的抑制作用中所起的作用。
